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Peripartum cardiomyopathy

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We read with great interest the review by Honigberg and Givertz. [1] The authors raised important questions, underlined gaps in our knowledge, and emphasized the fact that both the cause and mechanism of peripartum cardiomyopathy (PPCM) are unclear. Our most recent work may shed some light on certain points raised by Honigberg and Givertz. [1]

We modeled PPCM in induced pluripotent stem cell (iPSC)-derived cardiomyocytes (iCM) from women with a history of PPCM and healthy controls.2 Our findings questioned the prolactin theory and the use of prolactin antagonists in PPCM. [1] The prolactin theory was originally based on the observation that pregnant mice lacking the signal transducer and activator of transcription 3 (STAT3) in their cardiomyo¬cytes had increased expression of 16 kDa prolactin. These mice exhibited the PPCM phe¬notype. [1 3] In contrast to this theory, we found that iCM from women with PPCM have higher amounts of STAT3, compared with healthy controls, before and after beta-agonist stimulation.

Another new finding is related to the VEGF inhibitor soluble fms-like tyrosine kinase-1 (sFlt-1), a potential mediator of PPCM development. [1 4] In PPCM, the source of persistently raised sFlt-1 post-partum is currently unknown. [1] We show that iCMs from patients with a history of PPCM secret high amounts of sFlt-1 that eliminate the iCM secreted VEGF. Our finding could explain the high levels of sFlt-1 in PPCM after the placental source of sFlt-1 is removed.

Finally, we also found abnormal cytokine secretion from iCM in patients with PPCM in response to beta-agonist stimulation. This last finding could explain why the use of beta-agonists in PPCM could be detrimental.1 Overall, our recent findings together with the comprehensive review by Honigberg and Givertz1 should stimulate further research on the etiology, mechanism, and treatment of PPCM.

We read the excellent clinical review by Honigberg et al on “Peripartum cardiomyopathy” 1. In our experience often the multidisciplinary planning for these patients involve cardiology, obstetrics and anesthesiology teams 2. Based on existing evidence it is mostly agreed upon, as the authors also mention that vaginal delivery is acceptable and need for Cesarean section mostly arises from fetal indications. Often the question on table for us anesthesiologists is type of anesthetic: central neuroaxial versus general endotracheal, and the type of monitoring 3, 4, 5. As per American Heart Association (AHA) and European Society of Cardiology (ESC), clinically patients with congestive heart failure may be classified into four groups: Class I (Dry & Warm: Compensated); Class II (Dry & Cold: Hypo-perfused & Hypovolemic); Class III (Wet & Warm: Congested & Well perfused) and Class IV (Wet & Cold: Congested & Hypo-perfused) 6. We would like to reiterate that unless it is emergent, usually central neuroaxial anesthesia (combined spinal epidural or epidural) works well for patients in Class I and also maybe in Class II & III. For those in Class IV, priority would be medical optimization with diuretics, vasopressors and inotropes. If a patient in Class IV needs an urgent C-section, probably general anesthesia may be considered given the ongoing decompensated status of the patient. Monitoring may be again based on the Clinical Class of the patient, ie, Class IV might need arterial line and central line whereas Class I to III might not. Also, non-invasive hemodynamic monitoring like bioreactance (NICOM) may be utilized 7. For extremes, intra-aortic balloon pump (IABP) have also been used 8.